ArticleProceedings of the National Academy of Sciences of the United States of America2017
Loss of mouse cardiomyocyte talin-1 and talin-2 leads to β-1 integrin reduction, costameric instability, and dilated cardiomyopathy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Meta-Analysis of 26 638 Individuals Identifies Two Genetic Loci Associated With Left Ventricular Ejection Fraction.Circulation. Genomic and precision medicine · 2020Pooled it
- ALY688 Protects Against Myocardial Ischemia-Reperfusion Injury via Direct Effects and Rab8a-Dependent Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
- A versatile AuNPs@UiO-66-based electrochemiluminescent immunosensing platform for sensitive detection of talin proteins.Mikrochimica acta · 2026Article
- Regulation of Pacemaker Current in the Sinoatrial Node by Zonula Occludens-1.bioRxiv : the preprint server for biology · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Talin1 loss activates DRG neurons to accelerate bone remodeling and fracture healing in mice.Journal of orthopaedic translation · 2026Article
- The talin1-p53 axis inhibits osteocyte senescence to promote bone mass and mediate skeletal adaptation to mechanical stimulation.Theranostics · 2026Article
- Signaling pathway alterations in hearts of a porcine model harboring a β-myosin heavy chain (MYH7-R403Q) gene variant.Journal of molecular and cellular cardiology plus · 2025Article
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Cardiomyocyte SORBS2 expression increases in heart failure and regulates integrin interactions and extracellular matrix composition.Cardiovascular research · 2025Article
- Disulfidptosis-Related Genes as Novel Biomarkers and Therapeutic Targets in Dilated Cardiomyopathy.Journal of inflammation research · 2025Article
- Focal Adhesion's Role in Cardiomyocytes Function: From Cardiomyogenesis to Mechanotransduction.Cells · 2024Review
- Genetic determinants of blood pressure and heart rate identified through ENU-induced mutagenesis with automated meiotic mapping.Science advances · 2024Article
- Characterization of genomic regions escaping epigenetic reprogramming in sheep.Environmental epigenetics · 2024Article
- Single-cell transcriptional landscape of long non-coding RNAs orchestrating mouse heart development.Cell death & disease · 2023Article
- Talin2 and KANK2 functionally interact to regulate microtubule dynamics, paclitaxel sensitivity and cell migration in the MDA-MB-435S melanoma cell line.Cellular & molecular biology letters · 2023Article
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- FIBCD1 is an endocytic GAG receptor associated with a novel neurodevelopmental disorder.EMBO molecular medicine · 2022Article
- Focal adhesion-mediated cell anchoring and migration: from in vitro to in vivo.Development (Cambridge, England) · 2022Article
- Loss of talin in cardiac fibroblasts results in augmented ventricular cardiomyocyte hypertrophy in response to pressure overload.American journal of physiology. Heart and circulatory physiology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Continuous contraction-relaxation cycles of the heart require strong and stable connections of cardiac myocytes (CMs) with the extracellular matrix (ECM) to preserve sarcolemmal integrity. CM attachment to the ECM is mediated by integrin complexes localized at the muscle adhesion sites termed costameres. The ubiquitously expressed cytoskeletal protein talin (Tln) is a component of muscle costameres that links integrins ultimately to the sarcomere. There are two talin genes, Tln1 and Tln2. Here, we tested the function of these two Tln forms in myocardium where Tln2 is the dominant isoform in postnatal CMs. Surprisingly, global deletion of Tln2 in mice caused no structural or functional changes in heart, presumably because CM Tln1 became up-regulated. Tln2 loss increased integrin activation, although levels of the muscle-specific β1D-integrin isoform were reduced by 50%. With this result, we produced mice that had simultaneous loss of both CM Tln1 and Tln2 and found that cardiac dysfunction occurred by 4 wk with 100% mortality by 6 mo. β1D integrin and other costameric proteins were lost from the CMs, and membrane integrity was compromised. Given that integrin protein reduction occurred with Tln loss, rescue of the phenotype was attempted through transgenic integrin overexpression, but this could not restore WT CM integrin levels nor improve heart function. Our results show that CM Tln2 is essential for proper β1D-integrin expression and that Tln1 can substitute for Tln2 in preserving heart function, but that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dilated cardiomyopathy.
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